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NUR 326 > Degenerative Muscle Disorders > Flashcards

Degenerative Muscle Disorders Flashcards

1
Q

what are synovial joints

A

movable joints

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2
Q

what are synovial joints composed of

A

outer fibrous capsule
interior synovial fluid
articular cartilage
synovial fluid

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3
Q

what is the function of a synovial joint

A

provide smooth surface and lubrication at the place where bones come together to prevent friction

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4
Q

what is OA

A

degeneration of joints caused by aging and stresses

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5
Q

what is causing in increase in OA

A

obesity and aging

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6
Q

what joints are most commonly affected by OA

A

cervical spine
lumbosacral spine
hip
knee
hand
first metatarsal phalangeal joint
spare wrist, elbow, ankle

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7
Q

what are the risk factors for OA

A

obesity
aging
hx of team sports, trauma/overuse
heavy occupational work
misalignment (women have wider hips)

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8
Q

etiology of OA

A

degradation of cartilage due to
- excessive loading of healthy joints
- normal loading of previously injured joints
stress applied at wt bearing joints

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9
Q

what is the patho of OA

A
  • pressure wears away cartilage, exposing subchondral bone that results in the development of cysts
  • cysts move through cartilage inc damage
  • chondrocytes will synthesize proteoglycans to repair cartilage which results in swelling from excess fluid
  • localized inflammation occurs inc damage again
  • osteoblasts are activated creating bony spurs and inc thickness of synovial fluid
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10
Q

as OA progresses, what happens to proteoglycans

A

they decrease

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11
Q

what does the loss of cartilage lead to

A

narrowing of the joint space

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12
Q

what are the 3 major things that happen with OA

A
  • bone: formation of bone spurs
  • cartilage: dec number of chondrocytes, so dec in cartilage repair
  • synovial fluid: thickens due to the inc in inflammatory response
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13
Q

what are osetophytes

A

small bony projection that develop along the rim of bone adjacent to cartilage loss

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14
Q

what is the hallmark of OA

A

osteophytes

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15
Q

what are the sx of OA

A

deep achy joint pain: inc w exertion, better at rest
pain during colder weather
stiffness in AM
crepitus w moving
joint swelling
altered gait
limited range of motion

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16
Q

what is the physical exam for OA

A

joint deformities and tenderness
dec ROM
fingers (late stage)
- herbeden’s nodes
- bouchard’s nodes

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17
Q

what are herbeden’s nodes

A

swelling at the distal interphalangeal joint

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18
Q

what are bouchard’s nodes

A

swelling at proximal interphalangeal joint

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19
Q

what are OA treatment goals

A

manage pain
maintain mobility
minimize disability

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20
Q

what pharm is used for OA

A

midl to moderate pain
- acetaminophen
- topical capsaicin
- NSAIDS
moderate to severe pain
- NSIADS (rx strength)
- NSIADS + colchicine
- Tylenol + tramadol
- opioids
- steroid injections

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21
Q

what is the MOA of NSAIDS

A

reduce the production of prostaglandins which are what promotes inflammation, pain, fever

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22
Q

what organ and system do NSAIDs potentially hurt the most

A

kidney
GI risk for bleeding

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23
Q

NSAIDs and the risk for bleeding

A
  • inc risk in older people
  • use caution if have had previous GI bleed or currently using anticoags
  • contraindicated for ppl w PUD
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24
Q

what are additional pharm therapies often used for OA

A
  • intra articular injection of glucocorticoids
  • dietary supplements: chondroitin sulfate, glucosamine
  • artifical joint fluid w hyaluronic acid
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25
Q

what is glucosamine sulfate

A

naturally occurring compound in body that helpd maintain cartilage health
- dec amount in body w age

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26
Q

what is chondroitin sulfate

A

naturally occurring chemical in cartilage that might slow doen cartilage breakdown

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27
Q

what is DDD

A

degenerative disc disease
- causes pain, motor weakness, neuropathy

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28
Q

where does DDD typically occur

A

lumbar and cervical spine

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29
Q

what is the patho of degenerative disc disease

A

intervertebral discs become dehydrated w age causing vertebral bones to become compressed which impinges on entering and exiting nerves
- causes dysfunction of motor and sensory spinal nerves impeding on movement and sensation of extremities
- weakness and paresthesia

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30
Q

what are s/s of lumbar DDD

A

pain in lower back that radiates down back of legs
pain in buttock/thighs
pain that worsens when sitting, bending, lifting, twisting
pain that is minimized when walking, changing positions, lying down
numbness, tingling, foot drop, weakness

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31
Q

what are the s/s of cervical DDD

A

chronic pain that radiates to shoulders and down arms
weakness and tingling/weakness in arm/hand

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32
Q

what is rheumatoid arthritis

A

systemic, auto immune, inflammatory condition of the synovium that causes
- pain
- limitation of movement
- destruction or erosion of joints, ligaments, muscles

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33
Q

what type of reaction are rheumatoid arthritis and lupus

A

type III

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34
Q

why does RA occur

A

unknown
- genetic factors and env links
- maybe an inappropriate immune response to joint injury

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35
Q

what are risk factors of RA

A

40-60
women
tobacco use

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36
Q

what is the patho of RA

A

autoimmune attack on synovial tissue
- cells activated are lymphocytes and macrophages which produce RH

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37
Q

what is RF

A

rheumatoid factor
- auto antibody against the body’s own antibody - IgG which forms immune complexes and activates complement –> deposits into tissue and causes damage

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38
Q

what is RA diagnosed

A

measure serum levels of RF

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39
Q

what happens as RA progresses

A

intensifying inflammatory response causes
- cartilage destruction by osteoclasts
- pannus formation

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40
Q

what is pannus

A

an extra growth of the joints that is vascularized and able to get nutrients
- causes: bone erosion, bone cysts, fissure development

41
Q

what are early clinical manifestations of RA

A

vague
- fatigue, anorexia, generalized stiffness

42
Q

what are later manifestations of RA

A

symmetrical pain, stiffness, motion limitations
inflammation: heat, swelling, tenderness

43
Q

what are the advanced characteristics of RA

A

deformities and disabilities
joint subluxation

44
Q

what is joint subluxation

A

the bone gets displaced bc the joint loses contact with articulating surface

45
Q

how is RA systemic?

A

causes fatigue and malaise
- potentially affects all/any body systems
most common
- rheumatoid nodules
- sjogrens syndrome

46
Q

what are rheumatoid nodules

A

immune mediated granulomas that develop around inflamed joints and in lungs
- subcutaneous and firm, necrotic core
- sometimes painful

47
Q

what are the goals of pharm for RA

A

relieve pain and swelling
slow or stop disease progression

48
Q

what pharm is used for RA

A

NSAIDs: immediate relief
Glucocorticoids: short term only
DMARDS

49
Q

what is lupus

A

autoimmune inflammatory disease that attacks the DNA’s own body
- multiple organ system
- acute flare up
- unpredictable

50
Q

what are the two forms of lupus

A
  • discoid: disease targets the skin
  • systemic: disease targets internal organs
51
Q

what type of sensitivity is lupus

A

type III

52
Q

what are the predisposing factors for SLE

A

genetic factors
female
20-40
african american
env triggers like UV rays
allergy to abx
hormonal factors –> oral contraceptives
tobacco use

53
Q

what is the SLE patho

A

B lymphocytes are hyperactive and produce antibodies called antinuclear antibody (ANA)
- when ANA are activated they attack DNA
- form immune complexes in tissues causing an inflammatory response that destroys tissue

54
Q

what are SLE manifestations (broad)

A

extreme fatigue
photosensitivity
butterfly rash
fever
wt change
unusual hair loss
edema
raynauds

55
Q

what are the multisystemic manifestations of SLE

A

CNS: h/a, dizzy, seizures, stroke
lungs: pleuritis, pleural effusions
heart: myocarditis, endocarditis
kidneys: nephritis
blood vessels: vasculitis
blood: anemia, leukopenia, thrombocytopenia, blood clots
Joints: arthritis

56
Q

what is a SLE flare

A

SLE characterized by exacerbations and remissions
- flare = acute exacerbation

57
Q

what are the warning signs of flares

A

fatigue
pain
headache

58
Q

what are ways to prevent flares

A

recognize warning signs and avoid triggers like
- sunlight exposure
- infection
- abruptly stopping meds
- stress

59
Q

what is sjogren syndrome

A

autoimmune destruction of any moisture producing gland
- enlarged gland with dec function
- lacrimal gland is dec tears
- salivary gland is dec papilla

60
Q

what is the pharm used for SLE

A

relieve pain and swelling
slow or stop disease prevention
- NSAIDs, glucocorticoids, DMARDS

61
Q

why are corticosteroids used for RA and SLE

A

rapid suppression of inflammation
- aids if sx not relieved by NSAIDs or w/ a flare up
- not for long term therapy

62
Q

what is the class of methotrexate

A

DMARD, antineoplastic, anti-rheumatic
- folic acid antimetabolite

63
Q

what is the moa for methotrexate

A

immunosuppressive

64
Q

how is methotrexate administered

A

PO or SQ/IV weekly

65
Q

what are side effects of methotrexate

A

GI
bone marrow suppression
shortened life expectancy (CVD and cancer)
liver toxicity
destroys rapidly producing cells

66
Q

what are nursing implications for methotrexate

A

11 black box warnings
folic acid supplement is necessary
no alc, pregnant
teach s/s of infection and no notify provider

67
Q

what is hydroxychloroquine class

A

DMARD, antimalarial, antirheumatic agent

68
Q

what is the moa of hydroxychloroquine

A

unknown, maybe have anti inflammatory properties

69
Q

what is the indication of hydroxychloroquine

A

slow the progression of RA when used w another DMARD
- often alone or combo w methotrexate

70
Q

what are the side effects of hydroxychloroquine

A

retinopathy

71
Q

what are the similarities between RA and SLE

A
  • autoimmune
  • systemic inflammation
  • multiple body systems
  • pharm
72
Q

what are the differences between RA and SLE

A

RA affects joints and sometimes organs
SLE affects organs and sometimes joints

73
Q

what is gout

A

type of arthritis caused by the deposition of urate salts/crystals into the synovial fluid
- acute and painful inflammation

74
Q

what is chronic tophaceous gout?

A

advanced stage of gout characterized by white nodules composed of uric acid

75
Q

what is uric acid

A

waste product from purine metabolism

76
Q

what does purine contain

A

nitrogen containing compound

77
Q

what are sources of purines

A

alcohol
organ meat like liver
red meat
seafood, shell fish

78
Q

where are uric acid typically excreted by

A

kidneys

79
Q

what are predisposing factors of gout

A

male
genetics
diet
obesity
diuretic therapy + kidney insufficiency

80
Q

what is gout pathogenesis

A

elevated uric acids levels which accumulate in the body fluids
formation of urate crystals which deposit around the joints causing inflammation
result is gouty arthritis

81
Q

what are gouty arthritis manifestations

A

pain: intense, great toe, early manifestations
inflammation: edema, tenderness, redness
fever
malaise

82
Q

what are complications of gouty arthritis

A

urate kidney stones

83
Q

what is the pharm for gout

A

acute
- NSIADs
- corticosteroid therapy
- colchicine
prophylactic
- allopurinol
- colchicine
- probenecid

84
Q

what is allopurinol class

A

antigout

85
Q

what is the moa of allopurinol

A

inhibits production of uric acid

86
Q

what is the therapeutic use for allopurinol

A

gout prophylaxis

87
Q

what are the adverse effects of allopurinol

A

rash

88
Q

what interactions are we concerned for with allopurinol

A

hypoglycemic agents: causes inc insulin, which dec glucose
warfarin: inc risk of bleeding

89
Q

what are the nursing implications of allopurinol

A
  • can cause gastric irritation so take with food or milk
  • monitor urine uric acid level and glucose
  • takes 2-6 wks to see improvement
90
Q

what class is colchicine

A

anti inflammatory, anti gout

91
Q

what is the moa of colchicine

A

unknown, thought to inhibit leukocyte infiltration and disrupt cell division

92
Q

what is the therapeutic use of colchicine

A

gout flare ups and prophylaxis

93
Q

what are the adverse effects of colchicine

A

GI problems bc they are rapid reproducing cells also
- typically the first sign of drug toxicity so stop immediately

94
Q

what are nursing considerations for colchicine

A

usually given oral
contraindicated for renal disease
avoid grapefruit, alc, B12
check for other interactions: CYP3A4 inhibitors, anoxin, statins, etc

95
Q

what class is probenecid

A

uricosuric agent

96
Q

what is the moa of probenecid

A

inhibits reabsorption of uric acid in the kidneys, promoting excretion

97
Q

what are the therapeutic uses of probenecid

A

treats hyperuricemia with gout

98
Q

what are the side effects of probenecid

A

Gi upset
dizzy
h/a
kidney/liver impairment –> hematuria, color changes, output changes, wt gain, n/v
lots of drug interactions

NUR 326 (20 decks)

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